Microplastics are global menace-associated with respiratory damages. The objective of this study was to investigate the airway hyper-responsiveness (AHR) and inflammation induced by polystyrene microplastic (PSMPs) in male C57BL/6 mice and its modulation by ‘Bronchom’, an herbal medicine. For the study, animals were pre-treated with varying doses of Bronchom before 21-day exposure to PSMPs, followed by assessment of pulmonary damages. PSMPs exposure in mice significantly induced AHR to methacholine, represented by elevated respiratory resistance, and reduced lung compliance. PSMPs also induced influx of pro-inflammatory cells and release of pro-inflammatory mediators TNF-α, IL-1β, IL-5, IL-6 and MIP-2α in the bronchoalveolar lavage of PSMPs-exposed animals. Histopathological analysis confirmed leukocyte infiltration and mild fibrosis in the lung tissues of PSMPs-exposed animals. PSMPs-exposure also enhanced mRNA expression of pro-inflammatory biomarkers in lung tissues. Bronchom-treated mice showed significant protection against the PSMPs-induced AHR, inflammatory cell influx and cytokine expression, along with histopathological changes in dose-dependent manner. Pirfenidone used as a positive control showed beneficiary effects against PSMPs-induced respiratory distress. Interestingly, FTIR spectroscopy of the Bronchom-treated mice lung tissues indicated dose-dependent reduction in PSMPs-specific transmittance signatures, suggesting their reduced bioaccumulation. In human THP-1 macrophages, Bronchom also attenuated PSMPs-induced TNF-α and IL-6 cytokines release. Ultra-high-performance-liquid-chromatography-quadrupole time-of-flight mass spectrometry (UPLC-QToF-MS) identified 80 phytochemicals, associated with robust anti-inflammatory and anti-oxidant profile. These results indicated that Bronchom effectively mitigates PSMPs-induced respiratory distress-associated inflammation and PSMPs bioaccumulation in lung tissue, likely due to its rich phytochemical composition. This study highlights Bronchom as a promising herbal intervention against microplastic-associated pulmonary ailments.